Differentiating frontal lobe seizures from temporal lobe seizures.
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Epilepsy, Frontal Lobe↗
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Newly formed excitatory pathways provide a substrate for hyperexcitability in experimental temporal lobe epilepsy.
Temporal lobe epilepsy (TLE) in humans and animals is associated with axonal sprouting of glutamatergic neurons and neosynaptogenesis in the hippocampal formation. We examined whether this plasticity of excitatory pathways contributes to an increased level of glutamatergic excitation in the CA1 region of rats experiencing chronic spontaneous limbic seizures following kainic acid or pilocarpine treatment. In chronic cases, we report an extensive axonal sprouting of CA1 pyramidal neurons, with many axonal branches entering the pyramidal cell layer and stratum radiatum, regions that are not innervated by axonal collaterals of CA1 pyramidal neurons in control animals. Concurrently with this anatomical reorganization, a large increase of the spontaneous glutamatergic drive is observed in the dendrites and somata of CA1 pyramidal cells. Furthermore, electrical activation of the reorganized CA1 associational pathway evokes epileptiform bursts in CA1 pyramidal cells. These findings suggest that reactive plasticity could contribute to the hyperexcitability of CA1 pyramidal neurons and to the propagation of seizures in these two models of TLE.
Animals↗
Failure to replicate previously reported genetic associations with sporadic temporal lobe epilepsy: where to from here?
Temporal lobe epilepsy (TLE), traditionally thought to develop largely due to environmental factors, has recently become the focus of association studies in an effort to determine genetic risk factors. Here we examine all previous claims of association of genetic polymorphisms with TLE by attempting replication in a cohort of 339 TLE patients of European origin. We also examine if these variants contribute to other types of epilepsy by examination in a larger cohort of 752 patients representing a range of different epilepsies. We fail to clearly replicate any of the previously reported associations and also fail to show a role for these variants in the development of other forms of epilepsy. Although our results cannot definitively rule out a role for these genes, they do suggest that most and perhaps all of the previous associations are false positives. As has been the experience with other diseases, these results highlight the importance of larger sample sizes and replication. In TLE, it appears that collaboration before publication is the best option to increase sample size sufficiently in the short term. These general principles are applicable to other studies undertaken for common complex diseases.
Amyloid↗
Selective alterations in GABAA receptor subtypes in human temporal lobe epilepsy.
Temporal lobe epilepsy (TLE) is associated with impaired inhibitory neurotransmission. Studies in animal models suggest that GABA(A) receptor dysfunction contributes to epileptogenesis. To understand the mechanisms underlying TLE in humans, it is fundamental to determine whether and how GABA(A) receptor subtypes are altered. Furthermore, identifying novel receptor targets is a prerequisite for developing selective antiepileptic drugs. We have therefore analyzed subunit composition and distribution of the three major GABA(A) receptor subtypes immunohistochemically with subunit-specific antibodies (alpha1, alpha2, alpha3, beta2,3, and gamma2) in surgical specimens from TLE patients with hippocampal sclerosis (n = 16). Profound alterations in GABA(A) receptor subtype expression were observed when compared with control hippocampi (n = 10). Although decreased GABA(A) receptor subunit staining, reflecting cell loss, was observed in CA1, CA3, and hilus, the distinct neuron-specific expression pattern of the alpha-subunit variants observed in controls was markedly changed in surviving neurons. In granule cells, prominent upregulation mainly of the alpha2-subunit was seen on somata and apical dendrites with reduced labeling on basal dendrites. In CA2, differential rearrangement of all three alpha-subunits occurred. Moreover, there was layer-specific loss of alpha1-subunit-immunoreactive interneurons in hippocampus proper, whereas surviving interneurons exhibited extensive changes in dendritic morphology. Throughout, expression patterns of beta2,3- and gamma2-subunits largely followed those of alpha-subunit variants. These results demonstrate unique subtype-specific expression of GABA(A) receptors in human hippocampus. The significant reorganization of distinct receptor subtypes in surviving hippocampal neurons of TLE patients with hippocampal sclerosis underlines the potential for synaptic plasticity in the human GABA system.
Adolescent↗
Mental aspects of temporal lobe epilepsy. Follow-up of 74 patients after resection of a temporal lobe.
Psychiatric disorders were investigated in 74 patients with drug-resistant temporal lobe epilepsy (complex partial epilepsy). In all cases unilateral anterior temporal lobectomy had been performed during the period 1960-69. At follow-up in 1970-71, 45 patients were free from seizures, and in a further group of 15 patients seizure frequency had been substantially reduced. There were four postoperative deaths. Six patients were psychiatrically normal and had no history of any such disorder. Behavioural disturbances were observed in 55 patients. Before operation 11 patients displayed schizophrenia-like psychoses, and nine others became psychotic during follow-up. Fourteen patients attempted suicide on one or more occasions. Half the patients had diminished sexual drive. Improvement in psychiatric status was clearly correlated with relief from seizures and, in those cases with only a few or no seizures after operation, led directly to social rehabilitation. The presence or absence of a psychiatric disorder was not useful as a criterion for or against surgery.
Adolescent↗
Discriminating patients with frontal-lobe epilepsy and temporal-lobe epilepsy: utility of a multilevel design fluency test.
Patients with frontal-lobe epilepsy (FLE) or temporal-lobe epilepsy (TLE) and matched control participants were given a design fluency test that assessed nonverbal fluency and switching ability. Patients with FLE generated fewer designs in the switching condition relative to the TLE patients and controls, whereas group differences did not emerge in the basic fluency conditions. When the side of the seizure focus and the presence or absence of a structural lesion were considered in patients with FLE, only those with left-lesional FLE generated fewer designs than controls did in the switching condition. Furthermore, patients with left-lesional and nonlesional FLE produced a greater proportion of set-loss errors than did controls. These results indicate that patients with FLE are impaired when they must simultaneously generate new designs and engage in cognitive switching; however, the pattern of impairment may depend on the side of the seizure focus and the presence of a structural lesion.
Adult↗
The frontal lobes, basal ganglia, and temporal lobes as sites for schizophrenia.
Positron emission tomography studies with fluorodeoxyglucose in patients with schizophrenia are reviewed and findings in the frontal lobes, basal ganglia, and temporal lobes summarized from more than 20 published studies. Despite methodological and clinical population differences between studies, most reports indicate that patients with schizophrenia are more likely to be low in these areas than in the occipital lobe, cerebellum, or in white matter. This is consistent with blood flow and some neuroanatomical findings. Cluster analysis on our own sample suggests that patients may be low in all three areas rather than a pattern of three distinct clusters. Further study of individual symptom differences, medication effects, and of psychophysical tasks salient for these brain areas is indicated.
Basal Ganglia↗
Interictal regional slow activity in temporal lobe epilepsy correlates with lateral temporal hypometabolism as imaged with 18FDG PET: neurophysiological and metabolic implications.
OBJECTIVES: The phenomenon of interictal regional slow activity (IRSA) in temporal lobe epilepsy and its relation with cerebral glucose metabolism, clinical data, MRI, and histopathological findings was studied. METHODS: Interictal 18F-fluorodeoxyglucose positron emission tomography (FDG PET) was performed under continuous scalp EEG monitoring in 28 patients with temporal lobe epilepsy not associated with intracranial foreign tissue lesions, all of whom subsequently underwent resective surgery. Regions of interest (ROIs) were drawn according to a standard template. IRSA was considered lateralised when showing a 4:1 or greater ratio of predominance on one side. RESULTS: Sixteen patients (57%) had lateralised IRSA which was always ipsilateral to the resection and of maximal amplitude over the temporal areas. Its presence was significantly related to the presence of hypometabolism in the lateral temporal neocortex (p=0.0009). Logistic regression of the asymmetry indices for all measured cerebral regions confirmed a strong association between IRSA and decreased metabolism of the posterior lateral temporal neocortex only (p=0.009). No significant relation could be shown between slow activity and age at onset, duration of the epilepsy, seizure frequency, and MRI evidence for hippocampal atrophy. Furthermore, IRSA was not specifically related to mesial temporal sclerosis or any other pathology. CONCLUSIONS: Interictal regional slowing in patients with temporal lobe epilepsy not associated with a mass lesion is topographically related to the epileptogenic area and therefore has a reliable lateralising, and possibly localising, value. Its presence is irrelevant to the severity or chronicity of the epilepsy as well as to lateral deactivation secondary to neuronal loss in the mesial temporal structures. Although slow EEG activity is generally considered as a non-specific sign of functional disturbance, interictal regional slowing in temporal lobe epilepsy should be conceptualised as a distinct electrographic phenomenon which is directly related to the epileptogenic abnormality. The strong correlation between interictal regional slowing and lateral temporal hypometabolism suggests in turn that the second may delineate a field of reduced neuronal inhibition which can receive interictal and ictal propagation.
Adolescent↗
Ictal neocortical slowing in temporal lobe epilepsy.
BACKGROUND: Temporal lobe epilepsy (TLE) may affect brain regions outside the temporal lobe, causing impaired neocortical function during seizures. METHODS: The authors selected 11 consecutive patients with mesial TLE and hippocampal sclerosis who underwent intracranial EEG monitoring and had no seizures during a follow-up period of at least 1 year after temporal lobe resection. Secondarily generalized seizures were excluded, and up to three seizures were analyzed per patient (31 seizures total). Electrode contacts were assigned to one of nine cortical regions based on MRI surface reconstructions. EEG during seizures was analyzed for specific patterns including low-voltage fast (LVF), rhythmic polyspike, spike-wave, irregular slowing, and postictal suppression. RESULTS: Mesial and lateral temporal contacts on the side of seizure onset showed significant increases in ictal patterns such as LVF and polyspike activity, followed by postictal suppression. Bilateral frontal and ipsilateral parietal cortex exhibited large amplitude irregular slow waves during seizures. This frontoparietal slowing persisted into the postictal period. Perirolandic and occipital cortex were relatively spared. These EEG patterns were accompanied by bland staring, minor automatisms, and unresponsiveness or amnesia in the majority of patients studied. CONCLUSIONS: Prominent irregular slowing occurs in bilateral frontal and ipsilateral parietal association cortex during and after temporal lobe seizures. EEG slowing in the frontoparietal association cortex may signify physiologic impairment that contributes to widespread altered cerebral function during partial seizures.
Adolescent↗
Auditory processing in patients with temporal lobe epilepsy.
UNLABELLED: Temporal epilepsy, one of the most common presentation of this pathology, causes excessive electrical discharges in the area where we have the final station of the auditory pathway. Both the anatomical and functional integrity of the auditory pathway structures are essential for the correct processing of auditory stimuli. AIM: to check the Auditory Processing in patients with temporal lobe epilepsy regarding the auditory mechanisms of discrimination from sequential sounds and tone patterns, discrimination of the sound source direction and selective attention to verbal and nonverbal sounds. METHOD: eight individuals with temporal lobe epilepsy were assessed, after excluding those with non-confirmed diagnosis or with the focus of discharges not limited to this lobe. The evaluation was carried out through special auditory tests: Sound Localization Test, Duration Pattern Test, Digits Dichotic Test and Non-Verbal Dichotic Test. Their performances were compared to the performances of individuals without neurological diseases (case-control study). RESULTS: similar performances were observed between patients with temporal lobe epilepsy and the control group regarding the auditory mechanism of sound source direction discrimination. Comparing the other auditory mechanisms assessed, the patients with temporal lobe epilepsy presented worse results. CONCLUSION: individuals with temporal lobe epilepsy had more deficits in auditory processing than those without cortical damage.
Acoustic Stimulation↗
Recurrent spontaneous motor seizures after repeated low-dose systemic treatment with kainate: assessment of a rat model of temporal lobe epilepsy.
Human temporal lobe epilepsy is associated with complex partial seizures that can produce secondarily generalized seizures and motor convulsions. In some patients with temporal lobe epilepsy, the seizures and convulsions occur following a latent period after an initial injury and may progressively increase in frequency for much of the patient's life. Available animal models of temporal lobe epilepsy are produced by acute treatments that often have high mortality rates and/or are associated with a low proportion of animals developing spontaneous chronic motor seizures. In this study, rats were given multiple low-dose intraperitoneal (i.p.) injections of kainate in order to minimize the mortality rate usually associated with single high-dose injections. We tested the hypothesis that these kainate-treated rats consistently develop a chronic epileptic state (i.e. long-term occurrence of spontaneous, generalized seizures and motor convulsions) following a latent period after the initial treatment. Kainate (5 mg/kg per h, i.p.) was administered to rats every hour for several hours so that class III-V seizures were elicited for > or = 3 h, while control rats were treated similarly with saline. This treatment protocol had a relatively low mortality rate (15%). After acute treatment, rats were observed for the occurrence of motor seizures for 6-8 h/week. Nearly all of the kainate-treated rats (97%) had two or more spontaneous motor seizures months after treatment. With this observation protocol, the average latency for the first spontaneous motor seizure was 77+/-38 (+/-S.D.) days after treatment. Although variability was observed between rats, seizure frequency initially increased with time after treatment, and nearly all of the kainate-treated rats (91%) had spontaneous motor seizures until the time of euthanasia (i.e. 5-22 months after treatment). Therefore, multiple low-dose injections of kainate, which cause recurrent motor seizures for > or = 3 h, lead to the development of a chronic epileptic state that is characterized by (i) a latent period before the onset of chronic motor seizures, and (ii) a high but variable seizure frequency that initially increases with time after the first chronic seizure. This modification of the kainate-treatment protocol is efficient and relatively simple, and the properties of the chronic epileptic state appear similar to severe human temporal lobe epilepsy. Furthermore, the observation that seizure frequency initially increased as a function of time after kainate treatment supports the hypothesis that temporal lobe epilepsy can be a progressive syndrome.
Animals↗
Electro-clinical correlation in temporal lobe epilepsy with emphasis on inter-areal analysis of the temporal lobe.
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Electroencephalography↗
Double dissociation of memory capacities after bilateral occipital-lobe or medial temporal-lobe lesions.
Memory for recently encountered information can be reflected in conscious recall and recognition of that material, or in facilitated reprocessing of that material, an effect known as repetition priming. Repetition priming may be perceptual (form-based) or conceptual (meaning-based). A patient with bilateral occipital-lobe lesions (L.H.) and a patient with bilateral medial-temporal lobe lesions (H.M.) showed a double dissociation between visuoperceptual priming (impaired in L.H. and intact in H.M.) and visual recognition memory (intact in L.H. and impaired in H.M.). L.H. showed intact conceptual priming for visually presented words; his pattern of impaired visuoperceptual priming and intact conceptual priming is the reverse dissociation to that observed in prior studies of patients with Alzheimer's disease, in whom occipital cortices are relatively spared. These double dissociations suggest that a memory system localized to the occipital lobe mediates visuoperceptual priming effects, and that this system is independent of neural circuits mediating conceptual priming effects, and independent of the limbic-diencephalic system supporting conscious recognition of recently encountered information.
Adult↗
Medial temporal lobe neuronal damage in temporal and extratemporal lesional epilepsy.
OBJECTIVE: To assess the extent of medial temporal lobe (TL) abnormalities of the neuronal marker N-acetylaspartate (NAA) in TL and extra-TL lesional partial epilepsy, and to determine whether decreases in NAA are related to lesion location, to lesion pathology, or to the seizures themselves. METHODS: The authors studied 19 patients with intractable partial epilepsy and an isolated structural cerebral lesion (10 TL, 9 extra-TL; 10 cortical dysplasia [CD], 9 non-CD lesions). Proton MRS imaging was used to determine the average relative resonance intensity of NAA for the TL regions of the left and right hemispheres. Values less than two SDs below the mean of normal control subjects were considered abnormal. RESULTS: Fourteen patients (74%) had abnormally low NAA relative to creatine (NAA/Cr) in at least one TL. Three-way analysis of variance (ANOVA; lesion pathology, lesion location, side of NAA/Cr decrease) showed that ipsilateral NAA/Cr was lower than contralateral (p = 0. 04). Three-way ANOVA (lesion location, generalized tonic-clonic seizures, side of NAA/Cr decrease) showed that generalized tonic-clonic seizures were associated with lower TL NAA/Cr (p = 0. 02). Lesion location and pathology showed no main effect on the NAA-to-Cr ratio in either analysis (p > 0.05). Linear regression analyses between seizure duration and NAA/Cr decrease was not significant. CONCLUSION: The authors demonstrated abnormally low TL NAA/Cr in the majority of patients with structural cerebral lesions. This abnormality did not differ with lesion location or pathology. They propose that the altered function of neuronal networks by an isolated structural cerebral lesion results in remote "functional dual pathology."
Action Potentials↗
Structural abnormalities are similar in familial and nonfamilial mesial temporal lobe epilepsy.
BACKGROUND/OBJECTIVE: Diffuse temporal lobe abnormalities can be observed on MRI of patients with mesial temporal lobe epilepsy (MTLE). Our objective was to perform qualitative and quantitative analyses of temporal lobe structures in patients with familial MTLE (FMTLE) and nonfamilial MTLE. METHODS: Two groups of patients were ascertained: 67 FMTLE patients (14 with refractory seizures) and 30 patients with nonfamilial refractory MTLE. We performed qualitative analyses of MRI (with multiplanar reconstruction) and volumes of hippocampi and anterior temporal lobes in all patients, and in a normal control group of 23 individuals. We used the Chi-square test and ANOVA for statistical analyses. RESULTS: We identified anterior temporal lobe abnormalities by visual analysis in only 4% of FMTLE patients and atrophy of the anterior temporal lobe by volumetric analysis in 19%. In the group of nonfamilial MTLE patients we found anterior temporal lobe abnormalities by visual analysis in 17% of patients and anterior temporal lobe atrophy in 13%. Hippocampal atrophy was present in 90% of FMTLE and in 83% of nonfamilial MTLE. No signs of cortical dysplasia were observed. CONCLUSION: Anterior temporal lobe atrophy and other abnormalities outside the mesial portion of temporal lobes were infrequent in both familial and nonfamilial MTLE patients. Despite the genetic basis, hippocampal atrophy in FMTLE is not associated with other abnormalities outside the mesial temporal regions.
Adolescent↗
Neuroimaging evidence of progressive neuronal loss and dysfunction in temporal lobe epilepsy.
Whether temporal lobe epilepsy is the result of an isolated, early injury or whether there is ongoing neuronal dysfunction or loss due to seizures is often debated. We attempt to address this issue by using magnetic resonance techniques. Proton magnetic resonance spectroscopic imaging can detect and quantify focal neuronal dysfunction or loss based on reduced signals from the neuronal marker N-acetylaspartate (NAA), and magnetic resonance imaging (MRI)-based measurements of hippocampal volumes (MRIvol) can quantify the amount of atrophy in this structure. We performed magnetic resonance spectroscopic imaging and MRIvol in 82 consecutive patients with medically intractable temporal lobe epilepsy to determine whether there was a correlation between seizure frequency, or type or duration of epilepsy, with NAA to creatine (Cr) values or hippocampal volumes. Volumes and spectroscopic resonance intensities were categorized as to whether they were measured from the temporal lobe ipsilateral or contralateral to the predominant electroencephalographic focus. Ipsilateral and contralateral NAA/Cr was negatively correlated with duration of epilepsy. Hippocampal volumes were negatively correlated with duration ipsilaterally but not contralaterally. Frequency of complex partial seizures was not correlated with any of the magnetic resonance measures. However, patients with frequent generalized tonic-clonic seizures had lower NAA/Cr bilaterally and smaller hippocampal volumes ipsilaterally than patients with none or rare generalized tonic-clonic seizures. The results suggest that although an early, fixed injury may cause asymmetric temporal lobe damage, generalized seizures may also cause progressive neuronal dysfunction or loss.
Adult↗
The radiologic investigation of temporal lobe epilepsy. Value of high resolution CT with temporal orientated sections.
The value of high resolution computed tomography of the temporal lobes using temporal lobe orientated sections and intrathecal contrast is described. The results of this technique are correlated with the pathologic findings in 13 patients subsequently proven to have temporal lobe gliomas. These patients all presented with drug resistant temporal lobe epilepsy and underwent temporal lobectomy. This technique was successful in detecting the tumours in 11 of 13 patients. The average size of the tumours was just over 2 cm. The importance of detecting these small tumours is emphasised because of the profound effect this has on management.
Brain↗
Altered distribution of excitatory amino acid receptors in temporal lobe epilepsy.
In temporal lobe epilepsy, excitatory amino acid receptors in the hippocampus and temporal lobe may contribute to both increased excitability and vulnerability to excitotoxic damage. We used receptor autoradiography to examine the density of N-methyl-D-aspartate (NMDA) and kainic acid (KA) receptors in the hippocampus and parahippocampal gyrus obtained from five patients who had undergone anterior temporal lobectomy for the treatment of intractable seizures and from six control individuals, in which the hippocampus was obtained postmortem. Within the hippocampal formation, loss of [3H]KA and NMDA-sensitive L-[3H]glutamate binding was apparent in the sclerotic regions CA3, hilus, and CA1. In the subiculum and molecular layer of the denate gyrus, binding densities were maintained or even increased in some of the epileptic patients. A two-fold increase in L-[3H]glutamate binding, along with an increase in [3H]KA binding, was observed in the parahippocampal gyrus obtained from the epileptic patients. The results suggest that the vulnerability of the hippocampus in temporal lobe epilepsy may result, at least in part, from the presence of aberrant excitatory circuits in the parahippocampal gyrus.
Adult↗